A closed foramen ovale is formed after birth when two fetal structures, the septum secundum (“secundum”) and septum primum (“primum”), become fused and fibrose together. Usually, the fusion of these two anatomical structures occurs within the first two years of life ensuring the formation of a normal functioning heart. However, in about 25-27% of the general population, the secundum and the primum either do not fuse or the fusion is incomplete. As a result, a long tunnel-like opening will exist in the interatrial septum (“septum”) which allows communication between the right and left atrial chambers of the heart. This tunnel-like opening is a cardiac defect known as a PFO.
Normally, a PFO will be found near the fossa ovalis, an area of indentation on the right atrial side of the interatrial septum as illustrated in FIGS. 1A and 1B. In most circumstances, a PFO will remain functionally closed or “competent” and blood flow through the PFO will not occur due to the higher atrial pressures in the left atrium that serve to secure the flap-like primum against the secundum and interatrial septum, thereby closing the PFO. See FIGS. 1A and 1B. Nevertheless, in instances of physical exertion or when pressures are greater in the right atrium, inappropriate right-to-left shunting of blood can occur introducing venous blood and elements, such as clots or gas bubbles within the blood, into the left atrium and the systemic atrial system, posing serious health risks including: hemodynamic problems; cryptogenic strokes; venous-to-atrial gas embolism; migraines; and in some cases even death.
Traditionally, open chest surgery was required to suture or ligate closed a PFO. However, these procedures carry high attendant risks such as postoperative infection, long patient recovery, and significant patient discomfort and trauma. Less invasive, or minimally invasive, treatments are preferred and are currently being developed.
To date, most of these non-invasive, or minimally invasive, procedures involve the transcatheter implantation of various mechanical devices to close or occlude a PFO. See FIGS. 2A and 2B. That they are not well suited or designed for the long tunnel-like anatomical shape of a PFO, is a significant drawback of many PFO devices currently on the market including: the Cardia® PFO Closure Device, Amplatzer® PFO Occluder, and CardioSEAL® Septal Occlusion Device, just to name a few. As a result, device deformation and distortion is not uncommon and instances of mechanical failure, migration or even device dislodgement have been reported. Further, these devices can irritate the cardiac tissues at, or near, the implantation site, which in turn can potentially cause thromboembolic events, palpitations, and arrhythmias. Other reported complications include weakening, erosion, and tearing of the cardiac tissues around the implanted devices.
Yet another disadvantage of these mechanical devices is that the occlusion of the PFO is not instantaneous or complete immediately following implantation. Instead, occlusion and complete PFO closure requires subsequent endothelization of these devices. This endothelization process can be very gradual and can take several months or more to occur. Thus, “occlusion” of the PFO is not immediate but can be a rather slow and extended process.
Finally, the procedure to implant these devices can be technically complicated and cumbersome, requiring multiple attempts before the device can be appropriately and sufficiently delivered to the PFO. Accordingly, use of these devices may require long procedure times during which the patient must be kept under conscious sedation posing further risks to patients.
In light of these potentially serious drawbacks, new and improved non-invasive and/or minimally invasive methods, devices, and systems for the treatment of PFO, which either do not require the use of implantable devices or overcome some of the current shortcomings discussed above, are needed. The present invention meets these, as well as other, needs.